The effects of passive humidifier dead space on respiratory variables in paralyzed and spontaneously breathing patients

BACKGROUND: Passive humidifiers have gained acceptance in the intensive care unit because of their low cost, simple operation, and elimination of condensate from the breathing circuit. However, the additional dead space of these devices may adversely affect respiratory function in certain patients. This study evaluates the effects of passive humidifier dead space on respiratory function. METHODS: Two groups of patients were studied. The first group consisted of patients recovering from acute lung injury and breathing spontaneously on pressure support ventilation. The second group consisted of patients who were receiving controlled mechanical ventilation and were chemically paralyzed following operative procedures. All patients used 3 humidification devices in random order for one hour each. The devices were a heated humidifier (HH), a hygroscopic heat and moisture exchanger (HHME) with a dead space of 28 mL, and a heat and moisture exchanger (HME) with a dead space of 90 mL. During each measurement period the following were recorded: tidal volume, minute volume, respiratory frequency, oxygen consumption, carbon dioxide production, ratio of dead space volume to tidal volume (VD/VT), and blood gases. In the second group, intrinsic positive end-expiratory pressure was also measured. RESULTS: Addition of either of the passive humidifiers was associated with increased VD/VT. In spontaneously breathing patients, VD/VT increased from 59 +/- 13 (HH) to 62 +/- 13 (HHME) to 68 +/- 11% (HME) (p < 0.05). In these patients, constant alveolar ventilation was maintained as a result of increased respiratory frequency, from 22.1 +/- 6.6 breaths/min (HH) to 24.5 +/- 6.9 breaths/min (HHME) to 27.7 +/- 7.4 breaths/min (HME) (p < 0.05), and increased minute volume, from 9.1 +/- 3.5 L/min (HH) to 9.9 +/- 3.6 L/min (HHME) to 11.7 +/- 4.2 L/min (HME) (p < 0.05). There were no changes in blood gases or carbon dioxide production. In the paralyzed patient group, VD/VT increased from 54 +/- 12% (HH) to 56 +/- 10% (HHME) to 59 +/- 11% (HME) (p < 0.05) and arterial partial pressure of carbon dioxide (PaCO2) increased from 43.2 +/- 8.5 mm Hg (HH) to 43.9 +/- 8.7 mm Hg (HHME) to 46.8 +/- 11 mm Hg (HME) (p < 0.05). There were no changes in respiratory frequency, tidal volume, minute volume, carbon dioxide production, or intrinsic positive end-expiratory pressure. DISCUSSION: These findings suggest that use of passive humidifiers with increased dead space is associated with increased VD/VT. In spontaneously breathing patients this is associated with an increase in respiratory rate and minute volume to maintain constant alveolar ventilation. In paralyzed patients this is associated with a small but statistically significant increase in PaCO2. CONCLUSION: Clinicians should be aware that each type of passive humidifier has inherent dead space characteristics. Passive humidifiers with high dead space may negatively impact the respiratory function of spontaneously breathing patients or carbon dioxide retention in paralyzed patients. When choosing a passive humidifier, the device with the smallest dead space, but which meets the desired moisture output requirements, should be selected.     

Work of breathing during lung-protective ventilation in patients with acute lung injury and acute respiratory distress syndrome: a comparison between volume and pressure-regulated breathing modes

BACKGROUND: Pressure-control ventilation (PCV) and pressure-regulated volume-control (PRVC) ventilation are used during lung-protective ventilation because the high, variable, peak inspiratory flow rate (V (I)) may reduce patient work of breathing (WOB) more than the fixed V (I) of volume-control ventilation (VCV). Patient-triggered breaths during PCV and PRVC may result in excessive tidal volume (V(T)) delivery unless the inspiratory pressure is reduced, which in turn may decrease the peak V (I). We tested whether PCV and PRVC reduce WOB better than VCV with a high, fixed peak V (I) (75 L/min) while also maintaining a low V(T) target. METHODS: Fourteen nonconsecutive patients with acute lung injury or acute respiratory distress syndrome were studied prospectively, using a random presentation of ventilator modes in a crossover, repeated-measures design. A target V(T) of 6.4 + 0.5 mL/kg was set during VCV and PRVC. During PCV the inspiratory pressure was set to achieve the same V(T). WOB and other variables were measured with a pulmonary mechanics monitor (Bicore CP-100). RESULTS: There was a nonsignificant trend toward higher WOB (in J/L) during PCV (1.27 + 0.58 J/L) and PRVC (1.35 + 0.60 J/L), compared to VCV (1.09 + 0.59 J/L). While mean V(T) was not statistically different between modes, in 40% of patients, V(T) markedly exceeded the lung-protective ventilation target during PRVC and PCV. CONCLUSIONS: During lung-protective ventilation, PCV and PRVC offer no advantage in reducing WOB, compared to VCV with a high flow rate, and in some patients did not allow control of V(T) to be as precise.     

Humidification during invasive and noninvasive mechanical ventilation: 2012

We searched the MEDLINE, CINAHL, and Cochrane Library databases for articles published between January 1990 and December 2011. The update of this clinical practice guideline is based on 184 clinical trials and systematic reviews, and 10 articles investigating humidification during invasive and noninvasive mechanical ventilation. The following recommendations are made following the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) scoring system: 1. Humidification is recommended on every patient receiving invasive mechanical ventilation. 2. Active humidification is suggested for noninvasive mechanical ventilation, as it may improve adherence and comfort. 3. When providing active humidification to patients who are invasively ventilated, it is suggested that the device provide a humidity level between 33 mg H(2)O/L and 44 mg H(2)O/L and gas temperature between 34°C and 41°C at the circuit Y-piece, with a relative humidity of 100%. 4. When providing passive humidification to patients undergoing invasive mechanical ventilation, it is suggested that the HME provide a minimum of 30 mg H(2)O/L. 5. Passive humidification is not recommended for noninvasive mechanical ventilation. 6. When providing humidification to patients with low tidal volumes, such as when lung-protective ventilation strategies are used, HMEs are not recommended because they contribute additional dead space, which can increase the ventilation requirement and P(aCO(2)). 7. It is suggested that HMEs are not used as a prevention strategy for ventilator-associated pneumonia.     

Small dead space heat and moisture exchangers do not impede gas exchange during noninvasive ventilation: a comparison with a heated humidifier

Objective

Adverse respiratory and gasometrical effects have been described in patients with acute respiratory failure (ARF) undergoing noninvasive ventilation (NIV) with standard heat and moisture exchangers (HME). We decided to evaluate respiratory parameters and arterial blood gases (ABG) of patients during NIV with small dead space HME compared with heated humidifier (HH).

Design

Prospective randomized crossover study.

Setting

A 16-bed medical intensive care unit (ICU).

Patients

Fifty patients receiving NIV for ARF.

Measurements

The effects of HME and HH on respiratory rate, minute ventilation, EtCO₂, oxygen saturation, airway occlusion pressure at 0.1 s, ABG, and comfort perception were compared during two randomly determined NIV periods of 30 min. The relative impact of HME and HH on these parameters was successively compared with or without addition of a flex tube (40 and 10 patients, respectively).

Main results

No difference was observed between HME and HH regarding any of the studied parameters, whether or not a flex tube was added.

Conclusion

If one decides to humidify patients’ airways during NIV, one may do so with small dead space HME or HH without altering respiratory parameters.     

Comparison of the effects of heat and moisture exchangers and heated humidifiers on ventilation and gas exchange during non-invasive ventilation

OBJECTIVE: To compare the short-term effects of a heat and moisture exchanger (HME) and a heated humidifier (HH) during non-invasive ventilation (NIV). DESIGN: Prospective, clinical investigation. SETTING: Intensive care unit of a university hospital. PATIENTS: Twenty-four patients with acute respiratory failure (ARF). INTERVENTION: Each patient was studied with a HME and a HH in a random order during two consecutive 20min periods of NIV. MEASUREMENTS AND RESULTS: Respiratory rate (RR), expiratory tidal volume (VTe) and expiratory minute ventilation (VE) were measured during the last 5 min of each period and blood gases were measured. Mean pressure support and positive end-expiratory pressure levels were, respectively, 15+/-4 and 6+/-2 cmH(2)O. VE was significantly greater with HME than with HH (14.8+/-4.8 vs 13.2+/-4.3 l/min; p<0.001). This increase in VE was the result of a greater RR for HME than for HH (26.5+/-10.6 vs 24.1+/-9.8 breaths/min; p=0.002), whereas the VT for HME was similar to that for HH (674+/-156 vs 643+/-148 ml; p=0.09). Arterial partial pressure of carbon dioxide (PaCO(2)) was significantly higher with a HME than with a HH (43.4+/-8.9 vs 40.8+/-8.2 mmHg; p<0.005), without significantly changing oxygenation. CONCLUSION: During NIV the increased dead space of a HME can negatively affect ventilatory function and gas exchange. The effect of HME dead space may decrease efficiency of NIV in patients with ARF.     

Respiratory controversies in the critical care setting. Does high-frequency ventilation offer benefits over conventional ventilation in adult patients with acute respiratory distress syndrome?

High-frequency ventilation is the application of mechanical ventilation with a respiratory rate > 100 breaths/min. High-frequency oscillatory ventilation (HFOV) is the form of high-frequency ventilation most widely used in adult critical care. The principles of lung-protective ventilation have matured in parallel with the technology for HFOV. The 2 basic principles of lung-protective ventilation are the use of small tidal volume and maintenance of adequate alveolar recruitment. Research in animal models and humans demonstrate that HFOV can support gas exchange with much smaller tidal volume than can be achieved with conventional ventilation. HFOV also provides more effective lung recruitment than conventional mechanical ventilation. However, at present, evidence is lacking that survival in adults with acute respiratory distress syndrome is improved by HFOV. Although HFOV may improve P(aO(2)) in some patients, this improvement is often transitory. Available evidence does not support that pulmonary inflammation is reduced with HFOV in adult acute respiratory distress syndrome. Heavy sedation and often paralysis are necessary. The promise of HFOV as a lung-protective ventilation strategy remains attractive, but additional clinical trials are needed to determine whether this approach is superior to lung-protective ventilation with conventional mechanical ventilation.     

The effects of dexmedetomidine on the ventilatory response to hypercapnia in rabbits

OBJECTIVE: Dexmedetomidine is a highly selective alpha(2)-adrenergic agonist that can reduce anesthetic requirements. This study, to assess its effect on respiration, examined the effects of various doses of dexmedetomidine (1, 10, 30 and 50 microg/kg) on the respiratory response to carbon dioxide (CO(2)) breathing in rabbits. DESIGN: Randomized prospective study. SETTING: Animal laboratory at a university school of medicine. INTERVENTION: From 28 animals, four groups of seven were randomly assigned to receive different doses of dexmedetomidine (groups D1, D10, D30 and D50). Under inhalation of sevoflurane, each animal was tracheostomized and intubated with a 4 mm internal diameter (i.d.) endotracheal tube. MEASUREMENTS AND RESULTS: After end-tidal sevoflurane concentration had decreased below 0.03% and during quiet breathing (QB); respiratory rate (RR), tidal volume (V(T)) and inspiratory time (T(I)) were measured, from which minute ventilation (MV) and mean inspiratory flow (V(T)/T(I)) were calculated. After these measurements had been completed, each animal breathed the balloon gas (5% CO(2) and 95% O(2)) until the end-tidal CO(2) (ETCO(2)) reached 10%. The respiratory measurements were repeated during the latter period. After the collection of these data, dexmedetomidine was infused intravenously and the same measurements were repeated 15 and 45 min after dexmedetomidine infusion. The slope of the ventilatory response to hypercapnia in D50 was significantly higher compared with D30 animals. In the range 1-30 microg/kg, during both QB and at 10% ETCO(2), MV was decreased in a dose-dependent manner. Dexmedetomidine depressed both V(T) and RR during QB and at 10% ETCO(2). CONCLUSION: Dexmedetomidine depressed resting ventilation and the respiratory response to CO(2), but it did not induce profound hypoxemia or hypercapnia in rabbits.     

Implementation of a low tidal volume ventilation protocol for patients with acute lung injury or acute respiratory distress syndrome

The ARDS (acute respiratory distress syndrome) Network study found 22% lower mortality in acute lung injury and ARDS patients ventilated with low tidal volumes (V(T)) than in those ventilated with traditional V(T) ventilation. Several points should be considered when using the low V(T) protocol for clinical practice. Prior to implementation, hemodynamic and acid-base status, minute ventilation, and adequacy of sedation should be assessed to minimize the potential for intolerance. The volume-preset, assist-control mode is recommended for better control of V(T), and the respiratory rate should be increased as V(T) is reduced, so as to maintain minute ventilation and prevent acute hypercapnia. When unavoidable, hypercapnia should be induced slowly. Ventilator inspiratory flow (V(I)) and trigger sensitivity settings should be optimized to limit the increase in work of breathing and dyspnea. When dyspnea results in double-triggered breaths, V(T) can be titrated to 7-8 mL/kg, provided end-inspiratory plateau pressure is < or = 30 cm H(2)O. In severe acidosis (pH < 7.15) V(T) also can be increased. However, every effort should be made to maintain plateau pressure and V(T) goals by buffering severe acidosis and treating patient-ventilator asynchrony with sedation. Evaluation for weaning should occur when adequate oxygenation can be maintained on 40% oxygen and a positive end-expiratory pressure of 8 cm H(2)O. Pressure support levels between 5 and 20 cm H(2)O (above 5 cm H(2)O positive end-expiratory pressure) are used for weaning and titrated to keep the respiratory rate < 35 breaths/min. Pressure support levels should be weaned aggressively, as long as the protocol's weaning tolerance criteria can be maintained.     

Patient-ventilator interactions during volume-support ventilation: asynchrony and tidal volume instability--a report of three cases

During pressure-support ventilation, tidal volume (V(T)) can vary according to the level of the patient's respiratory effort and modifications of the thoraco-pulmonary mechanics. To keep V(T) as constant as possible, the Siemens Servo 300 ventilator proposes an original modification of pressure-support ventilation, called volume-support ventilation (VSV). VSV is a pressure-limited mode of ventilation that uses V(T) as a feedback control: the pressure support level is continuously adjusted to deliver a preset V(T). Thus, the ventilator adapts the inspiratory pressure level, breath by breath, to changes in the patient's inspiratory effort and the mechanical thoraco-pulmonary properties. The clinician sets V(T) and respiratory frequency, and the ventilator calculates a preset minute volume. It has been shown that ineffective respiratory efforts can occur during pressure-support ventilation.     

Lung collapse during low tidal volume ventilation in acute respiratory distress syndrome

BACKGROUND: Current ventilator management for acute respiratory distress syndrome (ARDS) incorporates low tidal volume (V(T)) ventilation in order to limit ventilator-induced lung injury. Low V(T) ventilation in supine patients, without the use of intermittent hyperinflations, may cause small airway closure, progressive atelectasis, and secretion retention. Use of high positive end-expiratory pressure (PEEP) levels with low V(T) ventilation may not counter this effect, because regional differences in intra-abdominal hydrostatic pressure may diminish the volume-stabilizing effects of PEEP. CASE SUMMARY: A 35-year-old man with abdominal compartment syndrome (intra-abdominal pressure > 48 cm H2O developed ARDS and was treated with V(T) of 4.5 mL/kg and PEEP of 20 cm H2O. Despite aggressive fluid therapy, appropriate airway humidification and tracheal suctioning, the patient developed complete bronchial obstruction, involving the entire right lung and left upper lobe. After bronchoscopy the patient was placed on a higher V(T) (7.0 mL/kg). Intermittent PEEP was instituted at 30 cm H2O for 2 breaths every 3 minutes. This intermittently raised the end-inspiratory plateau pressure from 38 cm H2O to 50 cm H2O. With the same airway humidity and tracheal suctioning practices bronchial obstruction did not reoccur. CONCLUSION: Low V(T) ventilation in ARDS may increase the risk of small airway closure and retained secretions. This adverse effect highlights the importance of pulmonary hygiene measures in ARDS during lung-protective ventilation.     

Aspiration of dead space in the management of chronic obstructive pulmonary disease patients with respiratory failure

INTRODUCTION: Carbon dioxide clearance can be improved by reducing respiratory dead space or by increasing the clearance of carbon-dioxide-laden expiratory gas from the dead space. Aspiration of dead space (ASPIDS) improves carbon dioxide clearance by suctioning out (during expiration) the carbon-dioxide-rich expiratory gas while replacing the suctioned-out gas with oxygenated gas. We hypothesized that ASPIDS would allow lower tidal volume and thus reduce exposure to potentially injurious airway pressures. METHODS: With 8 hemodynamically stable, normothermic, ventilated patients suffering severe chronic obstructive pulmonary disease we tested the dead-space-clearance effects of ASPIDS. We compared ASPIDS to phasic tracheal gas insufflation (PTGI) during conventional mechanical ventilation and during permissive hypercapnia, which was induced by decreasing tidal volume by 30%. The mean P(aCO(2)) reductions with PTGI flows of 4.0 and 6.0 L/min and during ASPIDS (at 4.0 L/min) were 32.7%, 51.8%, and 53.5%, respectively. Peak, plateau, and mean airway pressure during permissive hypercapnia were significantly lower than during conventional mechanical ventilation but PTGI increased peak, plateau, and mean airway pressure. However, pressures were decreased during permissive hypercapnia while applying ASPIDS. Intrinsic positive end-expiratory pressure also increased with PTGI, but ASPIDS had no obvious influence on intrinsic positive end-expiratory pressure. ASPIDS had no effect on cardiovascular status. CONCLUSIONS: ASPIDS is a simple adjunct to mechanical ventilation that can decrease P(aCO(2)) during conventional mechanical ventilation and permissive hypercapnia.     

Gastric mucosal systemic partial pressure of carbon dioxide (PCO2) gradient in experimental endotoxin shock in swine – comparison of two methods

OBJECTIVES: Clinically applicable methods for continuous monitoring of visceral perfusion/metabolism do not exist. Gastric mucosal end-tidal partial pressure of carbon dioxide (PCO(2)) gradient has been used, but it has limitations, especially in patients with lung injury and increased dead space ventilation. We studied the agreement between gastric mucosal end-tidal (DPCO(2gas)) and gastric mucosal arterial PCO(2) (D((t-a))PCO(2)) gradients, and especially the effect of dead space ventilation (V(d)/V(t) ratio) on the agreement. We hypothesized that DPCO(2gas) can be used as a semi-continuous indicator of mucosal arterial PCO(2) gradient in sepsis. DESIGN: A randomized, controlled animal experiment. SETTING: National laboratory animal center. INTERVENTIONS: Twelvehour infusion of endotoxin in landrace pigs. MEASUREMENTS AND RESULTS: We measured end-tidal PCO(2) continuously, gastric mucosal PCO(2) every 10 min (gas tonometry) and arterial PCO(2) every 120 min. Carbon dioxide production and the V(d)/V(t) ratio were determined by indirect calorimetry. In the endotoxin group ( n=7) cardiac index increased and systemic vascular resistance decreased. Endotoxemia increased dead space ventilation by 27% ( p=0.001). Both DPCO(2gas) and D((t-a))PCO(2)increased significantly in the endotoxin group ( p<0.0001 and p=0.049, respectively). Control animals remained stable throughout the experiment. When we compared DPCO(2gas) and D((t-a))PCO(2)(Bland-Altman analysis), the bias and precision were 0.9 and 0.9 kPa in the control group and 2.0 and 2.2 kPa in the endotoxin group, respectively. The disagreement between DPCO(2gas) and D((t-a))PCO(2) increased as the V(d)/V(t) ratio increased. CONCLUSIONS: DPCO(2gas) is a clinically applicable method for continuous monitoring of visceral perfusion/metabolism. Septic lung injury and increased dead space ventilation decrease the accuracy of the method, but this may not be clinically important.     

Adoption of lower tidal volume ventilation improves with feedback and education

OBJECTIVE: To determine whether feedback and education improve adoption of lung-protective mechanical ventilation (ie, with lower tidal volume [V(T)]). METHODS: We conducted a retrospective study of ventilator settings; we used data from 3 consecutive studies of patients with acute lung injury and/or acute respiratory distress syndrome, in the intensive care units of 2 university hospitals in the Netherlands. At site 1 we conducted a time series study of before and after education and feedback about lung-protective mechanical ventilation, and we compared the results from site 1 to the ventilation strategies used at site 2, which did not undergo the education and feedback intervention. Feedback and education consisted of presentations of actual ventilator settings, advised ventilator settings, and discussions on potential reasons for not using lower V(T). RESULTS: Two studies were performed at site 1, in 1999-2000 (Study 1, n = 22) and in 2002 (Study 2, n = 12). In 2003-2004, Study 3 was performed simultaneously at site 1 (n = 8) and site 2 (n = 17). At site 1, the mean +/- SD V(T) was 10.9 mL/kg predicted body weight (PBW) (95% CI 10.3-11.6) in Study 1 and 9.9 mL/kg PBW (95% CI 9.0-10.8) in Study 2 (difference not significant). After the feedback and education intervention at site 1, V(T) declined to 7.6 mL/kg PBW (95% CI 6.5-8.7) in Study 3 (p = 0.003). At site 2, where no feedback or education were given, V(T) was 10.3 mL/kg PBW (95% CI 9.5-11.0) in Study 3 (p < 0.001 vs Site 1). CONCLUSIONS: Adoption of a lower-V(T) ventilation strategy in patients with acute lung injury or acute respiratory distress syndrome is far from complete in the Netherlands. Adoption of a lower-V(T) strategy improves after feedback and education.     

Effect of the humidification device on the work of breathing during noninvasive ventilation

OBJECTIVE: Heat and moisture exchangers (HME) increase circuitry deadspace compared to heated humidifiers (HH). This study compared the effect of HH and HME during noninvasive ventilation (NIV) on arterial blood gases and patient's effort assessed by respiratory muscles pressure-time product and by work of breathing (WOB). DESIGN AND SETTING: Randomized cross-over study in a medical intensive care unit. PATIENTS: Nine patients receiving NIV for moderate to severe acute hypercapnic respiratory failure. MEASUREMENTS: HME was randomly compared to HH during periods of 20 min. Each device was studied without (ZEEP) and with a PEEP of 5 cmH(2)O. At the end of each period arterial blood gases, ventilatory parameters, oesophageal and gastric pressures were recorded and indexes of patient's effort calculated. RESULTS: Minute ventilation was significantly higher with HME than with HH (ZEEP: 15.8+/-3.7 vs. 12.8+/-3.6 l/min) despite a similar PaCO(2) (60+/-16 vs. 57+/-16 mmHg). HME was associated with a greater increase in WOB (ZEEP: 15.5+/-7.7 vs. 8.4+/-4.5 J/min and PEEP: 11.3+/-5.7 vs. 7.3+/-3.8 J/min) and indexes of patient effort. NIV with HME failed to decrease WOB compared to baseline. Addition of PEEP reduced the level of effort, but similar differences between HME and HH were observed. CONCLUSIONS: In patients receiving NIV for moderate to severe acute hypercapnic respiratory failure, the use of HME lessens the efficacy of NIV in reducing effort compared to HH.     

Accuracy of physiologic dead space measurements in patients with acute respiratory distress syndrome using volumetric capnography: comparison with the metabolic monitor method

BACKGROUND: Volumetric capnography is an alternative method of measuring expired carbon dioxide partial pressure (P(eCO2)) and physiologic dead-space-to-tidal-volume ratio (V(D)/V(T)) during mechanical ventilation. In this method, P(eCO2) is measured at the Y-adapter of the ventilator circuit, thus eliminating the effects of compression volume contamination and the need to apply a correction factor. We investigated the accuracy of volumetric capnography in measuring V(D)/V(T), compared to both uncorrected and corrected measurements, using a metabolic monitor in patients with acute respiratory distress syndrome (ARDS). METHODS: There were 90 measurements of V(D)/V(T) made in 23 patients with ARDS. The P(eCO2) was measured during a 5-min expired-gas collection period with a Delta-trac metabolic monitor, and was corrected for compression volume contamination using a standard formula. Simultaneous measurements of P(eCO2) and V(D)/V(T) were obtained using volumetric capnography. RESULTS: V(D)/V(T) measured by volumetric capnography was strongly correlated with both the uncorrected (r2 = 0.93, p < 0.0001) and corrected (r2 = 0.89, p < 0.0001) measurements of V(D)/V(T) made using the metabolic monitor technique. Measurements of V(D)/V(T) made with volumetric capnography had a bias of 0.02 and a precision of 0.05 when compared to the V(D)/V(T) corrected for estimated compression volume contamination. CONCLUSION: Volumetric capnography measurements of V(D)/V(T) in mechanically-ventilated patients with ARDS are as accurate as those obtained by metabolic monitor technique. .     

Barriers to providing lung-protective ventilation to patients with acute lung injury

OBJECTIVE: No studies have explored the barriers to implementing lung-protective ventilation in patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Our objective was to identify barriers to using lung-protective ventilation in patients with ALI/ARDS. DESIGN: Survey with content analysis of open-ended responses. SETTING: Medical center. PARTICIPANTS: Experienced intensive care unit nurses and respiratory therapists network identified through purposive sampling at hospitals from the ARDS Network, a National Institutes of Health-sponsored research consortium. INTERVENTIONS: Survey. RESULTS: Fifty-five surveys representing all ten ARDS Network sites were received. Twenty-seven (49%) of the respondents were intensive care unit nurses, 24 (44%) were respiratory therapists, and four did not indicate their profession. Clinicians had used lung-protective ventilation in a median of 20 (interquartile range, 10-50) patients with ALI/ARDS. Respondents identified physician willingness to relinquish control of ventilator, physician recognition of ALI/ARDS, and physician perceptions of patient contraindications to low tidal volumes as important barriers to initiating lung-protective ventilation. Important barriers to continuing patients on lung-protective ventilation were concerns over patient discomfort and tachypnea and concerns over hypercapnia, acidosis, and hypoxemia. Techniques for overcoming barriers were identified including specific ventilator setup recommendations, clinician education, and tools to assess patient discomfort. CONCLUSIONS: Experienced bedside clinicians perceive important barriers to implementing lung-protective ventilation. Successful strategies to increase use of lung-protective ventilation should target these barriers.     

Aspiration of dead space allows isocapnic low tidal volume ventilation in acute lung injury. Relationships to gas exchange and mechanics

OBJECTIVE: In acute lung injury (ALI) mechanical ventilation damages lungs. We hypothesised that aspiration and replacement of dead space during expiration (ASPIDS) allows normocapnic ventilation at higher end-expiratory pressure (PEEP) and reduced tidal volume (V(T)), peak and plateau pressures (Paw(peak), Paw(plat)), thus avoiding lung damage. SETTING: University Hospital. PATIENTS: Seven consecutive sedated and paralysed ALI patients were studied. Interventions and measurements: Single breath test for CO(2) and multiple elastic pressure volume (Pel/V) curves recorded from different end-expiratory pressures guided ventilatory setting at ASPIDS. ASPIDS was studied at respiratory rate (RR) of 14 min(-1) and then 20 min(-1) with minute ventilation maintaining stable CO(2) elimination. RESULTS: Alveolar and airway dead spaces were 24.3% and 31.3% of V(T), respectively. Multiple Pel/V curves showed a shift towards lower volume at decreasing PEEP, thus indicating that patients required a higher PEEP. At ASPIDS, PEEP was increased from 8.9 cmH(2)O to 12.6 cmH(2)O and VT reduced from 11 ml/kg to 8.9 ml/kg at RR 14 min(-1) and to 6.9 ml/kg at RR 20 min(-1). A significant decrease in Paw(peak) (36.7 vs 32 at RR 14 min(-1) and 28.7 at RR 20 min(-1)) and Paw(plat) (29.9 vs 27.3 at RR 14 min-1 and 24.1 at RR 20 min-1) were observed. PaCO(2) remained stable. No intrinsic PEEP developed. No side effects were noticed. CONCLUSIONS: ASPIDS allowed the use of higher PEEP at lower V(T) and inflation pressure and constant PaCO(2). Multiple Pel/V curves gave insight into the tendency of lungs to collapse.     

Index / Index

Humidification of gases delivered to patients is always necessary during invasive mechanical ventilation (with a minimum humidity of 30 mg H₂O/l) and most often during noninvasive ventilation (there is currently no clear recommendation on the humidity level required in this situation). Heat and moisture exchangers (HME) and heated humidifiers (HH) can be used. Contrary to usual belief, HH are not always the most efficient to humidify gases. Clinicians should be aware that in some situations (high temperature in the room or sun directly on the humidifier), gases are not sufficiently humidified and there is no efficient monitoring of the moisture currently proposed routinely. Before choosing a HME to humidify the gases, the very heterogeneous humidity performance of the devices proposed on the market must be known. Their humidification performance is reduced mainly in case of hypothermia. Their other limitation is the additional dead space that reduces CO₂ elimination during controlled mechanical ventilation, especially in situations where the respiratory rate is high and the tidal volumes low (as in acute respiratory distress syndrome, ARDS). During spontaneous ventilation, this additional dead space may increase the respiratory work of breathing. This may be compensated by an increase in pressure support levels especially during weaning tests. Based on the analysis of the various data in the literature, we recommend the use of HME as first-line, following the contra-indications (especially hypothermia). The heated humidifiers should be used in case of protective ventilation, especially in ARDS.     

Patient-ventilator synchrony during pressure-targeted versus flow-targeted small tidal volume assisted ventilation

PURPOSE: Low tidal volume (V(T)) delivered by flow-targeted breaths reduces ventilator-induced lung injury but may increase patient breathing effort because of limited flow. We hypothesized that a variable-flow, pressure-targeted breath would improve breathing effort versus a fixed flow-targeted breath. MATERIALS AND METHODS: We compared pressure assist-control ventilation and volume assist-control ventilation (VACV) in 12 patients with acute respiratory failure receiving 6 to 8 mL/kg V(T). Backup frequency, V(T), inspiratory time, applied positive end-expiratory pressure and fraction of inspired oxygen were held constant. Patient breathing effort was assessed by airway pressure (Paw) drop below baseline 0.1 second after the breath initiation (P(0.1)), the maximal Paw drop during the triggering phase (Ptr), the magnitude of ventilator work during flow delivery, and the presence of an active expiratory effort during cycling and air trapping judged by the magnitude of residual flow at end-expiration. RESULTS: Compared with VACV, pressure assist-control ventilation decreased P(0.1), Ptr (by 25% and 16%, respectively), and evidence for trapped gas but not ventilator work during flow delivery or cycle dys-synchrony. Peak inspiratory flow was comparable between the 2 modes. CONCLUSIONS: In patients receiving small V(T) VACV with increased breathing effort, variable-flow, pressure-targeted ventilation may provide more comfort by decreasing respiratory drive during the triggering phase.